Date:
Nov 01, 1995

There is a growing body of evidence that a lack of sufficient oxygen to the infant during the birth period (the perinatal period) is not the major reason for the brain damage usually found in cerebral palsy; this is particularly true if the infant is full term (40 weeks) and of normal birth weight (5.5 lbs. or more). Studies indicate that less than 15% of cerebral palsy is attributable to insufficient oxygen at birth. It is believed that prenatal factors are the major reasons for developmental brain damage.

Attention has been drawn to a number of prenatal factors that influence fetal growth and development at different times in intra-uterine life. These prenatal factors are being identified and their influence studied as contributors to the damage of the developing brain resulting in cerebral palsy (see September 1995 Fact Sheet on Risk Factors and Causes). One contributor of importance is malfunction and/or pathology of the placenta. The placenta serves two major purposes:

• A selective filter between the circulation of the mother and the fetus; and
• A site for the storage, production and timely release of substances necessary for the growth and development of the fetus.

If these placental functions are seriously impaired, fetal growth and development are believed to be threatened, particularly brain development.

There are four major factors recognized at this time as causes of placental malfunction:

• poor placental structure and/or placement in the uterus
• infection of the placenta
• genetic and metabolic disorders of the mother
• inadequate blood supply to the placenta

In order to investigate the relationship of placental malfunction and the later development of cerebral palsy, studies will probably require the storing of placentas delivered at the time of birth of infants who are recognized to be at risk of developing cerebral palsy (e.g.: multiple births; poor muscle tone; respiratory distress; very low birth weight).

These infants can be followed and those who develop cerebral palsy identified. Following development of cerebral palsy, the stored placentas associated with the birth of these children can be examined anatomically, microscopically and biochemically. These findings can be compared to those from a sample of stored placentas from infants who did not develop cerebral palsy. The differences will provide the leads necessary to explore the role of the placenta in the development of cerebral palsy.

Because of this research area’s potential importance, the Foundation is stimulating needed research on the role of placental damage and/or malfunction in the development of cerebral palsy.

© UCP Research & Educational Foundation, November 1995